EsturgeonV1, Main, Exploration, bibRecordById, Pascal:09-0252976

Complete intracellular pH protection during extracellular pH depression is associated with hypercarbia tolerance in white sturgeon, Acipenser transmontanus

Identifieur interne : 000A15 ( Main/Exploration ); précédent : 000A14; suivant : 000A16

Complete intracellular pH protection during extracellular pH depression is associated with hypercarbia tolerance in white sturgeon, Acipenser transmontanus

Auteurs : D. W. Baker [Canada] ; V. Matey [États-Unis] ; K. T. Huynh [Canada] ; J. M. Wilson [Portugal] ; J. D. Morgan [Canada] ; C. J. Brauner [Canada]

Source :

American journal of physiology. Regulatory, integrative and comparative physiology [ 0363-6119 ] ; 2009.

RBID : Pascal:09-0252976

Descripteurs français

Pascal (Inist)
- Intracellulaire, pH, Protection, Extracellulaire, Tolérance, Pisces, Court terme, Sang, Plasma, Hydrogénocarbonate, Chlorure, Branchie, Dioxyde de carbone.

English descriptors

KwdEn :
- Acid-Base Equilibrium, Acidosis, Respiratory (metabolism), Acidosis, Respiratory (pathology), Acidosis, Respiratory (physiopathology), Adaptation, Physiological, Animals, Bicarbonates (metabolism), Blood, Brain (metabolism), Carbon Dioxide (blood), Carbon Dioxide (metabolism), Carbon dioxide, Chlorides, Chlorides (metabolism), Extracellular, Fishes, Gill, Gills (metabolism), Gills (physiopathology), Gills (ultrastructure), Hydrogen-Ion Concentration, Hydrogencarbonates, Hypercapnia (metabolism), Hypercapnia (pathology), Hypercapnia (physiopathology), Intracellular, Liver (metabolism), Muscle Fibers, Fast-Twitch (metabolism), Myocardium (metabolism), Pisces, Plasma, Protection, Proton-Translocating ATPases (metabolism), Short term, Sodium-Potassium-Exchanging ATPase (metabolism), Time Factors, Tolerance, pH.
MESH :
- chemical , blood : Carbon Dioxide.
- chemical , metabolism : Bicarbonates, Carbon Dioxide, Chlorides, Proton-Translocating ATPases, Sodium-Potassium-Exchanging ATPase.
- metabolism : Acidosis, Respiratory, Brain, Gills, Hypercapnia, Liver, Muscle Fibers, Fast-Twitch, Myocardium.
- pathology : Acidosis, Respiratory, Hypercapnia.
- physiopathology : Acidosis, Respiratory, Gills, Hypercapnia.
- ultrastructure : Gills.
- Acid-Base Equilibrium, Adaptation, Physiological, Animals, Fishes, Hydrogen-Ion Concentration, Time Factors.

Abstract

Sturgeons are among the most CO₂ tolerant of fishes investigated to date. However, the basis of this exceptional CO₂ tolerance is unknown. Here, white sturgeon, Acipenser transmontanus, were exposed to elevated CO₂ to investigate the mechanisms associated with short-term hypercarbia tolerance. During exposure to 1.5 kPa PCO₂, transient blood pH [extracellular pH (pHe)] depression was compensated within 24 h and associated with net plasma HCO^-₃ accumulation and equimolar Cl^- loss, and changes in gill morphology, such as a decrease in apical surface area of mitochondrial-rich cells. These findings indicate that pHe recovery at this level of hypercarbia is accomplished in a manner similar to most freshwater teleost species studied to date, although branchial mechanisms involved may differ. White sturgeon exposed to more severe hypercarbia (3 and 6 kPa PCO₂) for 48 h exhibited incomplete pH compensation in blood and red blood cells. Despite pHe depression, intracellular pH (pHi) of white muscle, heart, brain, and liver did not decrease during a transient (6 h of 1.5 kPa PCO₂) or prolonged (48 h at 3 and 6 kPa PCO₂) blood acidosis. This pHi protection was not due to high intrinsic buffering in tissues. Such tight active cellular regulation of pHi in the absence of pHe compensation represents a unique pattern for non-air-breathing fishes, and we hypothesize that it is the basis for the exceptional CO₂ tolerance of white sturgeon and, likely, other CO₂ tolerant fishes. Further research to elucidate the specific mechanisms responsible for this tremendous pH regulatory capacity in tissues of white sturgeon is warranted.

Affiliations:

Le document en format XML

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<term>Acidosis, Respiratory (metabolism)</term>
<term>Acidosis, Respiratory (pathology)</term>
<term>Acidosis, Respiratory (physiopathology)</term>
<term>Adaptation, Physiological</term>
<term>Animals</term>
<term>Bicarbonates (metabolism)</term>
<term>Blood</term>
<term>Brain (metabolism)</term>
<term>Carbon Dioxide (blood)</term>
<term>Carbon Dioxide (metabolism)</term>
<term>Carbon dioxide</term>
<term>Chlorides</term>
<term>Chlorides (metabolism)</term>
<term>Extracellular</term>
<term>Fishes</term>
<term>Gill</term>
<term>Gills (metabolism)</term>
<term>Gills (physiopathology)</term>
<term>Gills (ultrastructure)</term>
<term>Hydrogen-Ion Concentration</term>
<term>Hydrogencarbonates</term>
<term>Hypercapnia (metabolism)</term>
<term>Hypercapnia (pathology)</term>
<term>Hypercapnia (physiopathology)</term>
<term>Intracellular</term>
<term>Liver (metabolism)</term>
<term>Muscle Fibers, Fast-Twitch (metabolism)</term>
<term>Myocardium (metabolism)</term>
<term>Pisces</term>
<term>Plasma</term>
<term>Protection</term>
<term>Proton-Translocating ATPases (metabolism)</term>
<term>Short term</term>
<term>Sodium-Potassium-Exchanging ATPase (metabolism)</term>
<term>Time Factors</term>
<term>Tolerance</term>
<term>pH</term>
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</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Bicarbonates</term>
<term>Carbon Dioxide</term>
<term>Chlorides</term>
<term>Proton-Translocating ATPases</term>
<term>Sodium-Potassium-Exchanging ATPase</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Acidosis, Respiratory</term>
<term>Brain</term>
<term>Gills</term>
<term>Hypercapnia</term>
<term>Liver</term>
<term>Muscle Fibers, Fast-Twitch</term>
<term>Myocardium</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Acidosis, Respiratory</term>
<term>Hypercapnia</term>
</keywords>
<keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Acidosis, Respiratory</term>
<term>Gills</term>
<term>Hypercapnia</term>
</keywords>
<keywords scheme="MESH" qualifier="ultrastructure" xml:lang="en"><term>Gills</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Acid-Base Equilibrium</term>
<term>Adaptation, Physiological</term>
<term>Animals</term>
<term>Fishes</term>
<term>Hydrogen-Ion Concentration</term>
<term>Time Factors</term>
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<term>pH</term>
<term>Protection</term>
<term>Extracellulaire</term>
<term>Tolérance</term>
<term>Pisces</term>
<term>Court terme</term>
<term>Sang</term>
<term>Plasma</term>
<term>Hydrogénocarbonate</term>
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<front><div type="abstract" xml:lang="en">Sturgeons are among the most CO<sub>2</sub>
 tolerant of fishes investigated to date. However, the basis of this exceptional CO<sub>2</sub>
 tolerance is unknown. Here, white sturgeon, Acipenser transmontanus, were exposed to elevated CO<sub>2</sub>
 to investigate the mechanisms associated with short-term hypercarbia tolerance. During exposure to 1.5 kPa PCO<sub>2</sub>
, transient blood pH [extracellular pH (pHe)] depression was compensated within 24 h and associated with net plasma HCO<sup>-</sup>
<sub>3</sub>
 accumulation and equimolar Cl<sup>-</sup>
 loss, and changes in gill morphology, such as a decrease in apical surface area of mitochondrial-rich cells. These findings indicate that pHe recovery at this level of hypercarbia is accomplished in a manner similar to most freshwater teleost species studied to date, although branchial mechanisms involved may differ. White sturgeon exposed to more severe hypercarbia (3 and 6 kPa PCO<sub>2</sub>
) for 48 h exhibited incomplete pH compensation in blood and red blood cells. Despite pHe depression, intracellular pH (pHi) of white muscle, heart, brain, and liver did not decrease during a transient (6 h of 1.5 kPa PCO<sub>2</sub>
) or prolonged (48 h at 3 and 6 kPa PCO<sub>2</sub>
) blood acidosis. This pHi protection was not due to high intrinsic buffering in tissues. Such tight active cellular regulation of pHi in the absence of pHe compensation represents a unique pattern for non-air-breathing fishes, and we hypothesize that it is the basis for the exceptional CO<sub>2</sub>
 tolerance of white sturgeon and, likely, other CO<sub>2</sub>
 tolerant fishes. Further research to elucidate the specific mechanisms responsible for this tremendous pH regulatory capacity in tissues of white sturgeon is warranted.</div>
</front>
</TEI>
<affiliations><list><country><li>Canada</li>
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<li>États-Unis</li>
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<tree><country name="Canada"><noRegion><name sortKey="Baker, D W" sort="Baker, D W" uniqKey="Baker D" first="D. W." last="Baker">D. W. Baker</name>
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<name sortKey="Huynh, K T" sort="Huynh, K T" uniqKey="Huynh K" first="K. T." last="Huynh">K. T. Huynh</name>
<name sortKey="Morgan, J D" sort="Morgan, J D" uniqKey="Morgan J" first="J. D." last="Morgan">J. D. Morgan</name>
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<country name="Portugal"><noRegion><name sortKey="Wilson, J M" sort="Wilson, J M" uniqKey="Wilson J" first="J. M." last="Wilson">J. M. Wilson</name>
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</record>

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Complete intracellular pH protection during extracellular pH depression is associated with hypercarbia tolerance in white sturgeon, Acipenser transmontanus

Complete intracellular pH protection during extracellular pH depression is associated with hypercarbia tolerance in white sturgeon, Acipenser transmontanus

Source :

Descripteurs français

English descriptors

Abstract

Links toward previous steps (curation, corpus...)

Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

Pour mettre un lien sur cette page dans le réseau Wicri

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